Many patients with spinal cord injury (SCI) report moderate to severe chronic painful dysesthesias that remain refractory to typical clinical interventions. In rodent models of SCI, dorsal horn neurons become hyperexcitable and chronic pain syndromes develop. Recently, abnormal expression of voltage-gated sodium channels has been demonstrated to contribute to hyperexcitability in injured primary sensory neurons. Thus, this project is designed to expand this analysis to secondary sensory neurons in the spinal cord, i.e. to characterize the molecular basis for hyperexcitability of spinal dorsal horn neurons after injury through alterations in expression of voltage-gated sodium channels. Hypothesis 1: Temporal and spatial alterations in gene expression of voltage-gated sodium channels occurs within the spinal cord after contusion injury. Hypothesis 2: Altered expression of a candidate sodium channel contributes to the abnormal firing properties of dorsal horn neurons and chronic central pain behaviors after contusion injury. This project proposes an investigative strategy that combines molecular, immunohistochemical, electrophysiologic, and behavioral techniques to gain important and novel insights into the changes in sodium channel transcription that follow SCI, which likely contribute to the development of chronic central pain. The long-term goals are to identify clinically useful strategies for intervention and recovery after SCI.